Dr. Barnes did an extensive analysis of the autopsy records of people who died in Graz, Austria in the years 1930 and 1970, plus selected years in between â around 70,000 cases in all. Graz is a city with a stable population of around 230,000 people. There is only one hospital, the National Hospital (Landskrankenhaus), and by a two-hundred-year-old royal decree, everyone who dies in the National Hospital must have an autopsy. About seventy percent of deaths in Graz occur in the National Hospital.

Dr. Barnes noticed that during World War II, the incidence of death from coronary artery disease went almost to zero. After the war, that incidence went back to prewar levels. He believes people who would have died from heart attacks later in life died prematurely during the war â primarily from infectious diseases, because antibiotics were generally unavailable during that time. After the return of availability of antibiotics, the same people who would have died of infectious disease again began to die of coronary artery disease.

In the cases from the year 1930, the great majority of deaths in Graz were caused by tuberculosis. Tuberculosis kills its victims at the average age of forty (recall Wolfgang Amadeus Mozart â dead at age forty from tuberculosis).

Dr. Barnes is one of those people who thinks for himself. He looked at the evidence, as follows: prior to the era of antibiotics, coronary artery disease was almost unknown. A certain segment of the population was susceptible to tuberculosis and infections in general, and they died young from infectious disease, primarily tuberculosis. Then came antibiotics and an entirely new population of people appeared: people who were susceptible to both infection and to coronary artery disease; except now they were enabled to live long enough to die from the slower of the two diseases: coronary artery disease.

Coronary artery disease kills its victims at the average age of 66, 26 years later than the previous big killer, tuberculosis. Dr. Barnes noticed that the death rate from coronary artery disease in 1970 was ten times that of 1930. Statistically, the death rate would be expected to be double, not ten times the 1930 rate. The only way he could explain this to himself was that the people who were saved from tuberculosis were almost all dying of coronary artery disease, and the people who did not need saving from tuberculosis were not susceptible to coronary artery disease either. They would die at an older age of something else.

Dr. Barnes combined this insight with his vast clinical experience of thousands of people treated with thyroid replacement therapy and realized that the incidence of both infection and coronary artery disease is dramatically reduced by thyroid replacement. This led to the realization that thyroid deficiency is the common denominator in both susceptibility to infection and coronary artery disease. In other words, there is a segment of the population (about forty percent according to Dr. Barnes) which accounted for almost all deaths from infectious disease before the invention of antibiotics and is now destined to account for almost all of the mortality statistics related to heart attacks, and these same people are hypothyroid.

Dr. Barnes' advice to you is to take your morning basal temperature, and determine if you are one of those people and, if you are, find a doctor who will prescribe thyroid replacement therapy for you.

Ah, but there is the rub, for while the incidence of hypothyroidism was well appreciated before the invention of blood lab tests for the disease, now most doctors think it is rare. Remember, almost all doctors attend The Church of the Holy Lab Test on a regular basis. If the clinical picture presented by the patient conflicts with the Holy Lab Test, the clinical picture is ignored. According to this point of view, you cannot be hypothyroid unless you have a low T3 and/or T4 blood level.

So, if you have hypothyroidism, unless you have the proper lab result, you will have to become a discriminating consumer and conduct a search for a qualified physician. If I were you, I would call up armed with knowledge, and boldly ask to speak to the doctor before making an appointment. Ask the right questions. How common is hypothyroidism? Do you know about the taking of basal temperature? How reliable are lab tests in diagnosing hypothyroidism? Do you know of the work of Dr. Broda O. Barnes? Get the right answers or do not waste your time and money with that doctor.

If you think about it, Dr. Barnes' ideas dovetail nicely with what we now know about the mechanism of coronary, nay any, artery disease. We now believe this to be a free radical disease. Excess hydroxyl radicals left over from lipid peroxidation cause tiny areas of inflammation, then necrosis (tissue death), in the walls of arteries. When the body tries to repair this necrosis it forms a scar tissue and incorporates into the scar tissue calcium and cholesterol. The body's natural defense to this process is to produce antioxidants, which neutralize hydroxyl free radicals before they can do damage. Thyroid hormones regulate the rate of metabolism and, when in inadequate supply, the rate at which antioxidants are produced would, of course, be slower. Therefore, there would be less antioxidants around to do the job and atherosclerosis would proceed more rapidly.

It also makes sense that low thyroid function would make one susceptible to infection. The entire chemical factory we know as the immune system, is running only as fast as the amount of thyroid hormone which penetrates the immune system cells. Therefore, low thyroid _ depressed and slowed immunity _ increased likelihood of infection. It all fits together so well!

Hypothyroidism predisposes a person to arthritis, and thyroid replacement therapy often brings arthritic symptoms under control. In severe cases of arthritis it may be necessary to add a small dose of prednisone â from five mg. every other day up to five mg. twice daily. (I prefer natural hormones for hormone therapy, but this may be the one place prednisone, a synthetic hormone, should be used â only in low doses and only because the effect of cortisone treatment in arthritis wears off after a few days.) Some of the ill side effects of prednisone are due to its thyroid-suppressing effect and can be avoided, at least at low doses of prednisone, by supplementing thyroid hormone to the level required to maintain the basal temperature between 97.8 and 98.2.

Where gouty arthritis is concerned, thyroid replacement also helps here. Gout is caused by an inability to metabolize uric acid and the accumulation of uric acid, notably in the drainage system of the kidneys (as stones) and in the joints, especially the big toe. If the basal temperature (and thus the basal metabolic rate) is low, naturally the body is even less able to metabolize uric acid. Although thyroid replacement is not specific to gout, it is a valuable adjunct to the treatment of this painful disease.

Again the problem is that doctors rely on unreliable laboratory tests to determine the presence or absence of need for thyroid replacement therapy, when the only reliable test is the basal temperature.

The symptoms of diabetes are related to the poor control of blood sugar present in this disease due to either inadequate insulin production from the pancreas or a resistance in the cells of the body to the effect of insulin. It is as if, in some people, the body becomes immune to the effects of insulin. Before the discovery of insulin, the diagnosis of diabetes was a death sentence. The average person lived less than five years after diagnosis, and the usual cause of death was tuberculosis. One could say that part of being a diabetic was a weakness toward contracting and dying from tuberculosis.

Insulin was isolated by Canadian doctors Banting and Best in 1922, and for a few years the medical world was optimistic that diabetes would be cured. What happened instead was that controlling blood sugar with insulin allowed diabetics to live longer lives. This revealed aspects of diabetes, which previously had been no problem, because the diabetic died before they could appear. Diabetics were observed to develop atherosclerosis far earlier than non-diabetics, and this became the major killer of diabetics later in life, by heart attack or stroke. However, they die at a much younger average age than do other sufferers of atherosclerosis. It has been discovered that even before the onset of diabetes, the diabetic-to-be is developing atherosclerosis at an accelerated rate.

A weakness to tuberculosis and early atherosclerosis: just like hypothyroidism! And, indeed, if you check the diabetic for a low basal temperature, it often turns out that hypothyroidism is present. It has long been known that the classical test for diabetes, the GTT or glucose tolerance test, cannot distinguish between diabetes and hypothyroidism. However, sometimes doctors forget this and fail to collect the basal temperature (or worse yet rely on the T3/T4 tests) and thus treat hypothyroid patients for diabetes, which they do not have! Also, many true diabetics also have hypothyroidism, which is overlooked and not treated for the same reasons.

The complications of diabetes, such as cataracts, heart disease (and atherosclerosis in general) and kidney disease are not present in the diabetic, if that diabetic is producing plenty of thyroid hormone. These complications also can be prevented in the diabetic patient who also is hypothyroid, simply by adding thyroid replacement therapy. The point is that whenever diabetes is suspected, it should always be distinguished from hypothyroidism. This can be done by testing not only glucose tolerance but also insulin tolerance. A GTT should never be ordered alone. Second, even if a person is correctly diagnosed with diabetes, hypothyroidism should always be suspected anyway, and a basal temperature should be done with thyroid replacement, if indicated by a low reading. Many "prediabetics" are actually undiagnosed hypothyroid cases and, if not recognized as such, the opportunity to treat with thyroid and thus prevent atherosclerosis will be lost.

It appears from the extensive epidemiologic studies conducted by Broda Barnes on deaths occurring in Graz, Austria, that here are two other diseases to which there is a shared susceptibility, along with the susceptibility to tuberculosis, and those are lung cancer and emphysema. His data indicate that people who have tuberculosis are twenty times more likely also to have lung cancer than the average person.

As regards emphysema, part of the cause of this disease is chronic bronchitis, i.e., repeated infections of the bronchi. People who finally end up with emphysema are people who smoke and/or have had multiple infections of their breathing tubes. Infections produce coughing in the presence of obstruction of the airways by mucus. Coughing into obstructed lung tubes causes the pressure in those tubes to back up into the alveoli, the tiny sacs in the lungs where oxygen and carbon dioxide are exchanged. When the walls of these sacs rupture under pressure from coughing and scar tissue forms this is called "emphysema."

As we already have seen, people who are especially susceptible to infections are more likely to be hypothyroid, and the addition of thyroid replacement therapy raises resistance to infection to normal levels. This protects against bronchitis and therefore against the eventual development of emphysema.